Abstract
The anticancer effects of ceramide have been reported in many types of cancers but less in lung cancer. In this study, we used C2-ceramide to further investigate its possible anticancer effects and mechanisms on non-small cell lung cancer (NSCLC) H1299 cells. The result of cell proliferation in terms of trypan blue assay showed high dose of C2-ceramide inhibited cell survival after 24 h treatment. The flow cytometry-based assays indicated the effect of apoptosis, chromatin condensation, and G1 arrest in terms of Annexin V/propidium iodide (PI), DAPI, and PI stainings, respectively. Moreover, the decreased protein level of p-Akt, p-NFκB, survivin and cyclin A2 were detected by Western blot assay. Taken together, these results indicated the antiproliferative effect of C2-ceramide is majorly responsible for cell apoptosis in lung cancer H1299 cells.
Highlights
Approximately 80% of lung cancer belongs to nonsmall-cell lung cancer (NSCLC) and the other is SCLC histologically [1]
The proliferation rate of C2-ceramidetreated H1299 lung cancer cells significantly decreased in a dose–response manner (P < 0.001)
G1 arrest of C2-Ceramide-treated H1299 lung cancer cells The role of cell cycle interference in the C2-ceramideinduced apoptosis of H1299 lung cancer cells was examined by the flow cytometry-based propidium iodide (PI) assay (Figure 2)
Summary
80% of lung cancer belongs to nonsmall-cell lung cancer (NSCLC) and the other is SCLC histologically [1]. Smoking is one of the main risk factors for lung cancer [2], about 10% patients are non-smokers [3]. NSCLC is generally detected and diagnosed at late stage and its prognosis is poor [4]. The anticancer drugs for NSCLC treatment remain a challenge. Dysregulation of Akt was reported to be observed in various cancers including breast cancer [5] and lung cancer cells [6]. The constitutive activation of Akt has been shown to cause chemoresistant of cancer cells. NFκB, an inflammatory-associated transcription factor, is found to be constitutively activated
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